Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder characterized by excessive fat accumulation (steatosis, first hit) in the hepatic tissue, and it is mainly associated with insulin resistance, obesity, and type 2 diabetes (T2D). NAFLD can further advance to non-alcoholic steatohepatitis (NASH, multiple hit), and several hypotheses have been postulated for the progression from fatty liver to NASH, such as oxidative stress, lipid peroxidation in the liver, gut dysbiosis, impaired intestinal permeability, endotoxin-induced activation of hepatic stellate cells (HSCs), and mitochondrial dysfunction, which result in hepatic inflammation and fibrosis. Presently, the world is facing a huge challenge of pandemic scales to mitigate NASH because of its multifactorial etiology and unavailability of potential therapeutic agents. Furthermore, inflammation is a major driver for the progression of the disease from simple steatosis to hepatocellular carcinoma, an end-stage of liver disease. Moreover, NASH is associated with increased intestinal permeability that promotes the endotoxins to induce the secretion of inflammatory cytokines like TNF-a, IL-1ß, IL-6, and others. The inflammatory cascade ultimately triggers macrophage and HSC activation, thereby causing extracellular matrix (ECM) protein secretion and deposition of collagen, leading to liver fibrosis. These pieces of evidence signify the important concept of gut-liver crosstalk in NASH disease. Further, epigenetic changes can lead to aberrant expression of several genes responsible for gluconeogenesis, lipogenesis, and inflammation in the liver.
Moreover, there is a dearth of knowledge regarding how epigenetic mechanisms in the gut-liver axis are involved in NASH pathogenesis. Furthermore, NASH is an emerging global health threat that can progress gradually to cirrhosis and hepatocellular carcinoma, unfortunately, with no defined therapy. Therefore, the need of the hour is to identify novel therapeutic strategies.
We welcome submissions of original research, review, and mini-review focusing on but not limited to the following themes:
• Pathogenesis of NASH and its association with the gut axis
• The epigenetic mechanism involved in the pathogenesis of NASH
• Novel therapeutic strategies for the prevention of NASH
Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder characterized by excessive fat accumulation (steatosis, first hit) in the hepatic tissue, and it is mainly associated with insulin resistance, obesity, and type 2 diabetes (T2D). NAFLD can further advance to non-alcoholic steatohepatitis (NASH, multiple hit), and several hypotheses have been postulated for the progression from fatty liver to NASH, such as oxidative stress, lipid peroxidation in the liver, gut dysbiosis, impaired intestinal permeability, endotoxin-induced activation of hepatic stellate cells (HSCs), and mitochondrial dysfunction, which result in hepatic inflammation and fibrosis. Presently, the world is facing a huge challenge of pandemic scales to mitigate NASH because of its multifactorial etiology and unavailability of potential therapeutic agents. Furthermore, inflammation is a major driver for the progression of the disease from simple steatosis to hepatocellular carcinoma, an end-stage of liver disease. Moreover, NASH is associated with increased intestinal permeability that promotes the endotoxins to induce the secretion of inflammatory cytokines like TNF-a, IL-1ß, IL-6, and others. The inflammatory cascade ultimately triggers macrophage and HSC activation, thereby causing extracellular matrix (ECM) protein secretion and deposition of collagen, leading to liver fibrosis. These pieces of evidence signify the important concept of gut-liver crosstalk in NASH disease. Further, epigenetic changes can lead to aberrant expression of several genes responsible for gluconeogenesis, lipogenesis, and inflammation in the liver.
Moreover, there is a dearth of knowledge regarding how epigenetic mechanisms in the gut-liver axis are involved in NASH pathogenesis. Furthermore, NASH is an emerging global health threat that can progress gradually to cirrhosis and hepatocellular carcinoma, unfortunately, with no defined therapy. Therefore, the need of the hour is to identify novel therapeutic strategies.
We welcome submissions of original research, review, and mini-review focusing on but not limited to the following themes:
• Pathogenesis of NASH and its association with the gut axis
• The epigenetic mechanism involved in the pathogenesis of NASH
• Novel therapeutic strategies for the prevention of NASH